Screening,Monitoring,and Treatment of Stage 1to 3Chronic Kidney Disease:A Clinical Practice Guideline From the American College of Physicians
Amir Qaseem,MD,PhD,MHA;Robert H.Hopkins Jr.,MD;Donna E.Sweet,MD;Melissa Starkey,PhD;and Paul Shekelle,MD,PhD,for the Clinical Guidelines Committee of the American College of Physicians*
Description:The American College of Physicians (ACP)developed this guideline to present the evidence and provide clinical recom-mendations on the screening,monitoring,and treatment of adults with stage 1to 3chronic kidney disease.
Methods:This guideline is based on a systematic evidence review evaluating the published literature on this topic from 1985through November 2011that was identified by using MEDLINE and the Cochrane Database of Systematic Reviews.Searches were limited to English-language publications.The clinical outcomes evaluated for this guideline included all-cause mortality,cardiovascular mor-tality,myocardial infarction,stroke,chronic heart failure,composite vascular outcomes,composite renal outcomes,end-stage renal dis-ease,quality of life,physical function,and activities of daily living.This guideline grades the evidence and recommendations by using ACP’s clinical practice guidelines grading system.
Recommendation 1:ACP recommends against screening for chronic kidney disease in asymptomatic adults without risk factors for chronic kidney disease.(Grade:weak recommendation,low-quality evidence)
Recommendation 2:ACP recommends against testing for protein-uria in adults with or without diabetes who are currently taking an angiotensin-converting enzyme inhibitor or an angiotensin II–receptor blocker.(Grade:weak recommendation,low-quality evidence)
Recommendation 3:ACP recommends that clinicians select phar-macologic therapy that includes either an angiotensin-converting enzyme inhibitor (moderate-quality evidence)or an angiotensin II–receptor blocker (high-quality evidence)in patients with hyperten-sion and stage 1to 3chronic kidney disease.(Grade:strong recommendation)
Recommendation 4:ACP recommends that clinicians choose statin therapy to manage elevated low-density lipoprotein in patients with stage 1to 3chronic kidney disease.(Grade:strong recommenda-tion,moderate-quality evidence)
Ann Intern Med.2013;159:https://www.doczj.com/doc/9a7059207.html, For author affiliations,see end of text.
This article was published online first at https://www.doczj.com/doc/9a7059207.html, on 22October 2013.
C
hronic kidney disease (CKD)is nearly always asymp-tomatic in its early stages (1).The most commonly accepted de?nition of CKD was developed by Kidney Dis-ease:Improving Global Outcomes (KDIGO)(2)and the Kidney Disease Outcomes Quality Initiative (KDOQI)(3)as abnormalities of kidney structure or function,present for more than 3months,with implications for health.Cri-teria for CKD include markers of kidney damage (albu-minuria,as indicated by an albumin excretion rate of 30mg/24h or greater and an albumin–creatinine ratio of 3mg/mmol or greater [?30mg/g]);urine sediment abnor-malities;electrolyte and other abnormalities due to tubular disorders;abnormalities detected by histologic examina-tion;structural abnormalities detected by imaging;history of kidney transplantation or presence of kidney damage;or kidney dysfunction that persists for 3or more months,as shown by structural and functional abnormalities (most often based on increased albuminuria,as indicated by a urinary albumin–creatinine ratio of 3mg/mmol or greater
[?30mg/g])or a glomerular ?ltration rate (GFR)less than 60mL/min/1.73m 2for 3or more months.
Traditionally,CKD is categorized into 5stages that are based on disease severity de?ned by GFR (3)(Table 1);stages 1to 3are considered to be early-stage CKD.People with early stages of the disease are typically asymptomatic,and the diagnosis is made by using laboratory tests or im-aging.In 2013,KDIGO revised CKD staging to consider both 5stages of GFR as well as 3categories of albuminuria to de?ne CKD severity (2).
*This paper,written by Amir Qaseem,MD,PhD,MHA;Robert H.Hopkins Jr.,MD;Donna E.Sweet,MD;Melissa Starkey,PhD;and Paul Shekelle,MD,PhD,was developed for the Clinical Guidelines Committee of the American College of Physicians.Individuals who served on the Clinical Guidelines Committee from initiation of the project until its approval were Paul Shekelle,MD,PhD (Chair );Roger Chou,MD;Molly Cooke,MD;Paul Dallas,MD;Thomas D.Denberg,MD,PhD;Nick Fitterman,MD;Mary Ann Forciea,MD;Robert H.Hopkins Jr.,MD;Linda L.Humphrey,MD,MPH;Tanveer P.Mir,MD;Douglas K.Owens,MD,MS;Holger J.Schu ¨nemann,MD,PhD;Donna E.Sweet,MD;and Timothy Wilt,MD,MPH.Approved by the ACP Board of Regents on 17November 2012.
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Summary for Patients.......................I-28Web-Only CME
quiz
Approximately 11.1%(22.4million)of adults in the United States have stage 1to 3CKD,and prevalence ap-pears to be increasing,especially for stage 3CKD (4,5).Approximately one half of persons with CKD have either stage 1or 2CKD (increased albuminuria with normal GFR),and one half have stage 3CKD (low GFR,with one third of these individuals having increased albuminuria and two thirds having normal albuminuria)(5).The prevalence of CKD is slightly higher in women than in men (12.6%vs.9.7%)(6).
Stage 1to 3CKD,reduced GFR,and albuminuria are associated with mortality (7,8),cardiovascular disease (9),fractures (10),bone loss (11),infections (12),cognitive impairment (13),and frailty (14).Treatment of stage 1to 3CKD involves treating associated conditions and compli-cations.Many patients with CKD may already be taking medications targeting comorbid conditions,such as hyper-tension,cardiovascular disease,and diabetes.
This American College of Physicians (ACP)guideline presents available evidence on the screening,monitoring,and treatment of stage 1to 3CKD.Clinicians are the target audience.The target patient population for screen-ing is adults,and the target population for treatment it is adults with stage 1to 3CKD.
M ETHODS
This guideline is based on a systematic evidence review sponsored by the Agency for Healthcare Research and Quality (AHRQ)(15)and conducted by the Minnesota Evidence-based Practice Center (6)that addressed the fol-lowing key questions:
1.In asymptomatic adults with or without recognized risk factors for CKD incidence,progression,or complica-tions,what direct evidence is there that systematic CKD screening improves clinical outcomes?
2.What harms result from systematic CKD screening in asymptomatic adults with or without recognized risk factors for CKD incidence,progression,or complications?
3.Among adults with CKD stages 1to 3,whether detected by systematic screening or as part of routine care,what direct evidence is there that monitoring for worsening
kidney function or kidney damage improves clinical outcomes?
4.Among adults with CKD stages 1to 3,whether detected by systematic screening or as part of routine care,what harms result from monitoring for worsening kidney function or kidney damage?
5.Among adults with CKD stages 1to 3,whether detected by systematic screening or as part of routine care,what direct evidence is there that treatment improves clin-ical outcomes?
6.Among adults with CKD stages 1to 3,whether detected by systematic screening or as part of routine care,what harms result from treatment?
The literature search identi?ed randomized,controlled trials and controlled clinical trials published in English from 1985through November 2011,by using MEDLINE and the Cochrane Database of Systematic Reviews and re-view of reference lists of relevant articles and articles sug-gested by experts.Details of the evidence review methods are available in the full AHRQ report (6).
This guideline rates the recommendations by using the ACP’s guideline grading system (Table 2)(16).
R ISK F ACTORS
FOR
CKD
The major risk factors for CKD include diabetes,hy-pertension,and cardiovascular disease.Other risk factors include older age;obesity;family history;and African American,Native American,or Hispanic ethnicity.Diabe-tes is more prevalent in patients with stage 1to 3CKD (20%)than in patients without CKD (5%)(17).Hyper-tension is also more prevalent in patients with CKD (64%in stage 3and 36%in stage 1)than in patients without CKD (24%)(17).The prevalence of cardiovascular disease increased from 6%in patients without CKD to 36%in those with stage 3CKD (17).
S CREENING
FOR
CKD
Benefits of Screening
Direct Evidence
No randomized,controlled trials that compared the effect of systematic CKD screening versus no CKD screen-ing on clinical outcomes were identi?ed.
Indirect Evidence
Prevalence.Among U.S.adults older than 20years,11.1%have stage 1to 3CKD.Approximately 5%of adults younger than 52years and without diabetes,hyper-tension,or obesity have CKD,compared with 68%older than 81years (17).Most patients with stage 1to 3CKD are not clinically recognized to have CKD (18,19).
Adverse Health Consequences.Although stage 1to 3CKD is usually asymptomatic,it is associated with mortal-ity (7,8),cardiovascular disease (9),fractures (10),bone
CKD Stage Definition
1Kidney damage with GFR ?90mL/min/1.73m 2
2Kidney damage with GFR of 60–89mL/min/1.73m 23GFR of 30–59mL/min/1.73m 22
CKD ?chronic kidney disease;GFR ?glomerular ?ltration rate.
*Adapted from reference 3.The Kidney Disease:Improving Global Outcomes Work Group recently updated its de?nition of CKD progression to include con-sideration of both GFR and albuminuria stages (2).
Clinical Guideline
Screening,Monitoring,and Treatment of Stage 1to 3CKD
loss(11),infections(12),cognitive impairment(13),and frailty(14).
Validity and Reliability of Screening Tests.No popu-lation-based studies have tested the sensitivity or speci?city of1-time CKD screening using either estimated GFR or albuminuria or the validity and reliability of repeated screening.Serum creatinine is measured by using a simple blood test.Although no studies have compared GFR esti-mated from serum creatinine values with direct GFR mea-surement,estimation is believed to be reasonably accurate (20).There are many sources of variability when measuring urinary albumin loss(21),and the method of collection and measurement of urinary albumin and creatinine has yet to be standardized.
Effect of Treatments on Screen-Detected CKD.There was no randomized trial evidence evaluating the effective-ness of treatment on clinical outcomes of CKD identi?ed
through screening.
Harms of Screening
Direct Evidence
No randomized,controlled trials have evaluated the harms of systematic CKD screening.
Indirect Evidence
Expert opinion suggests that the harms of CKD screening include misclassi?cation of patients owing to false-positive test results,adverse effects of unnecessary test-ing,psychological effects of being labeled with CKD,ad-verse events associated with pharmacologic treatment changes after CKD diagnosis,and possible?nancial rami-?cations of CKD diagnosis.
M ONITORING FOR CKD
Benefits of Monitoring
Direct Evidence
No randomized,controlled trials have evaluated clini-cal outcomes for patients with stage1to3CKD who were systematically monitored for worsening kidney function versus no CKD monitoring,usual care,or an alternative CKD monitoring regimen.
Indirect Evidence
Frequency of Worsening of Kidney Function or Damage in Patients With Stage1to3CKD.The mean annual GFR decline in patients with CKD varies widely,ranging from approximately1to greater than10mL/min/1.73m2(3). Annual rates of conversion from microalbuminuria to macro-albuminuria range from2.8%to9%(22–27).Factors that have been shown to predict faster decline in GFR include diabetes,proteinuria,hypertension,older age,obesity,dys-lipidemia,smoking,male sex,and cause of primary kidney disease.
Association of CKD Progression With Adverse Health Consequences.No studies longitudinally assessed the risk for adverse health outcomes in patients with worsening CKD.A meta-analysis of prospective cohort studies reported risk for all-cause and cardiovascular mortality for different GFRs and degrees of albuminuria(8).Patients with albu-minuria and GFR greater than60mL/min/1.73m2(CKD stage1or2)had a higher mortality risk if they had mac-roalbuminuria compared with microalbuminuria,although lower GFR within this range was not associated with a higher mortality risk.Mortality risk was increased in pa-tients with a GFR of45to59mL/min/1.73m2,higher in those with GFR30to44mL/min/1.73m2,and even higher in those with GFR less than30mL/min/1.73m2.
Validity and Reliability of Tests to Monitor CKD Progression.The same tests are used both to screen for CKD and monitor its progression.No studies assessed the accuracy,precision,speci?city,or sensitivity of estimating GFR over time or for detecting a change in CKD stage on the basis of GFR category.The lack of consistent repro-ducibility in albuminuria measurements causes concern about the ability of longitudinal albuminuria measure-ments to accurately represent CKD progression.
Effect of Treatments on Clinical Outcomes in Patients Whose CKD Has Progressed.Evidence is lacking on whether treatments reduce the risk for adverse clinical out-comes in patients with worsening CKD.
Harms of Monitoring
Direct Evidence
No randomized,controlled trials were identi?ed that compared the adverse effects of systematic monitoring of stage1to3CKD versus no CKD monitoring,usual care, or an alternative CKD monitoring regimen.
Indirect Evidence
Expert opinion suggests that the harms of monitoring for CKD progression include incorrect reclassi?cation of patients,adverse effects of unnecessary testing,labeling ef-fects,adverse events associated with changes in pharmaco-logic treatments after testing,and possible?nancial rami-?cations of a more advanced CKD diagnosis.
*Adopted from the classi?cation developed by the GRADE(Grading of Recom-mendations,Assessment,Development,and Evaluation)workgroup.
Clinical Guideline
Screening,Monitoring,and Treatment of Stage1to3CKD
T REATMENT OF CKD
Table3summarizes the evidence on treatments for stage1to3CKD.
Antihypertensive Drugs
Monotherapy
Patients receiving?-blockers or calcium-channel blockers for CKD treatment may have received other con-comitant antihypertensive agents.
Angiotensin-Converting Enzyme Inhibitors Versus Place-bo.Nineteen studies compared treatment with angiotensin-converting enzyme(ACE)inhibitors with placebo in patients with stage1to3CKD(23–26,28–42). Moderate-quality evidence showed that treatment with ACE inhibitors reduced the risk for end-stage renal disease (ESRD)(relative risk[RR],0.65[95%CI,0.49to0.88]) compared with placebo in patients with stage1to3CKD (26–28,31,33–35,38).The risk for ESRD was not re-duced in patients with only microalbuminuria or impaired GFR.Moderate-quality evidence showed that treatment with ACE inhibitors did not reduce the risk for all-cause mortality compared with placebo(23–26,28–39,41)(Ta-ble3).Pooled data from10trials(23–26,29–31,35,36, 39)showed that mortality risk was reduced in patients with microalbuminuria(RR,0.79[CI,0.66to0.96]),although most of the data were derived from a large study that showed no difference in mortality between patients with and without microalbuminuria(43).Therapy with ACE inhibitors did not reduce the risk for cardiovascular mor-tality,myocardial infarction(MI),stroke,or other vascular outcomes.
ACE Inhibitors Versus?-Blockers.Low-quality evi-dence showed no difference in the risk for ESRD or all-cause mortality,cardiovascular mortality,stroke,or heart failure between patients treated with ACE inhibitor mono-therapy compared with?-blocker monotherapy(44–46) (Table3).
ACE Inhibitors Versus Diuretics.Low-quality evidence showed no difference between ACE inhibitor–treated and diuretic-treated patients in terms of risk for ESRD(47) (Table3).Evidence was insuf?cient evidence to determine whether the treatments alter the all-cause mortality risk. There was no statistically signi?cant difference between the 2treatments in risk for stroke or multiple composite car-diovascular outcomes.
ACE Inhibitors Versus Angiotensin II–Receptor Blockers.End-stage renal disease outcomes were not re-ported in studies comparing ACE inhibitor monotherapy with angiotensin II–receptor blocker(ARB)monotherapy. Low-quality evidence showed that there was no difference between these2monotherapies in risk for all-cause mor-tality(36,48–51)(Table3).There was no statistically signi?cant difference between the2treatments for other reported clinical vascular or renal outcomes.
ACE Inhibitors Versus Calcium-Channel Blockers.Low-quality evidence showed that there was no difference in the risk for ESRD(47,52,53)or all-cause mortality(23,52–56)between ACE inhibitor monotherapy and calcium-channel blocker monotherapy(Table3).There was also no difference between the2treatments in terms of risk for cardiovascular mortality,stroke,congestive heart failure (CHF),or any composite vascular end point.
ACE Inhibitors Versus Non–ACE Inhibitor Antihyper-tensive Therapy.Low-quality evidence showed that ACE inhibitor monotherapy did not statistically signi?cantly re-duce the risk for ESRD compared with non–ACE inhibi-tor antihypertensive therapy(calcium antagonists,?-blockers,or?-adrenoblockers)(57)(Table3).Evidence was insuf?cient that ACE inhibitor therapy compared with non–ACE inhibitor antihypertensive therapy is associated with a reduced risk for all-cause mortality.
ARB Monotherapy Versus Placebo.High-quality evi-dence showed that treatment with ARBs reduced the risk for ESRD in patients with stage1to3CKD(RR,0.77 [CI,0.66to0.90])compared with placebo(58–60).How-ever,it was not possible to determine whether risk was also reduced in patients with microalbuminuria or impaired GFR who do not have diabetes and hypertension(58–60). High-quality evidence showed that treatment with ARBs did not reduce the risk for all-cause mortality compared with placebo(58–61)(Table3).Treatment with ARBs did not reduce the risk for cardiovascular mortality,MI, CHF complications,or any other clinical vascular outcome compared with placebo;however,ARB treatment did sta-tistically signi?cantly improve renal outcomes.
ARBs Versus Calcium-Channel Blockers.Low-quality evidence showed that ARB monotherapy did not reduce the risk for ESRD(59)or all-cause mortality(59,62)com-pared with calcium-channel blocker monotherapy(Table 3).There was also no statistically signi?cant difference be-tween the2treatments in terms of risk for stroke,cardio-vascular mortality,CHF,or composite vascular end points.
?-Blockers Monotherapy Versus Placebo.End-stage re-nal disease outcomes were not reported in studies compar-ing?-blocker monotherapy with placebo.Moderate-quality evidence showed that treatment of CKD with a ?-blocker reduced the risk for all-cause mortality com-pared with placebo(RR,0.73[CI,0.65to0.82])(63–66).?-Blocker treatment also statistically signi?cantly reduced the risk for cardiovascular mortality(64,66),CHF hospi-talization(65,66),and CHF death(65,66).
Calcium-Channel Blockers Versus Placebo.Low-quality evidence showed that treatment with calcium-channel blockers in mostly hypertensive patients with albuminuria did not reduce the risk for ESRD(59)or all-cause mortal-ity(23,59)compared with placebo,although this treat-ment did reduce the risk for MI(23,59)(Table3).There was no statistically signi?cant reduction in composite renal outcomes.
Calcium-Channel Blockers Versus?-Blockers.Low-quality evidence showed that calcium-channel blocker monotherapy did not statistically signi?cantly reduce the
Clinical Guideline Screening,Monitoring,and Treatment of Stage1to3CKD
Intervention
Outcome
Strength of Evidence From RCTs (Reference)Result
Other Outcomes
Adverse Events*
ACE inhibitor vs.placebo Mortality
Moderate (23–26,28–39,41,42)No reduced risk overall (RR,0.91[95%CI,0.79to 1.05])
Reduced risk for composite renal outcomes;
mortality risk reduced in patients with microalbuminuria Cough
ESRD
Moderate (26–28,31,33–35,38)Reduced risk (RR,0.65[CI,0.49to 0.88])
ARB vs.placebo
Mortality High (58–61)No reduced risk (RR,1.04[CI,0.92to 1.18])Reduced risk for CHF hospitalization (1of 2trials reporting)and composite renal
outcomes (1of 3trials reporting)
Hyperkalemia
ESRD
High (58–61)
Reduced risk (RR,0.77[CI,0.6to 0.90])
ACE inhibitor vs.ARB Mortality Low (36,48–51)No reduced risk (RR,1.04[CI,0.37to 2.95])No reduced risk for other outcomes reported NR
ESRD Insufficient
NA
ACE inhibitor ?ARB vs.ACE inhibitor
Mortality Moderate (50,71,72)No reduced risk (RR,1.03[CI,0.91to 1.18])
Reduced risk for composite vascular outcomes
Increased risk for cough,
hyperkalemia,hypotension,and acute kidney failure requiring dialysis ESRD
Low (70)No reduced risk (RR,1.00[CI,0.15to 6.79])
ACE inhibitor ?ARB vs.ARB
Mortality Moderate?(60)No reduced risk (RR,1.02[CI,0.93to 1.13])
Reduced risk for composite vascular outcomes
NR
ESRD
Low?(60)No reduced risk (RR,1.19[CI,0.77to 1.85])?-Blocker vs.placebo Mortality Moderate (63–66)Reduced risk (RR,0.73[CI,0.65to 0.82])Reduced risk for CVD mortality,CHF
hospitalization,CHF death,and composite vascular outcomes Heart failure,fatigue,bradycardia,dizziness,and hypotension
ESRD
Insufficient
NA
Calcium-channel blocker vs.placebo
Mortality Low (23,59)No reduced risk (RR,0.90[CI,0.69to 1.19])
Reduced risk for MI
Hyperkalemia
ESRD
Low (59)No reduced risk (RR,1.03[CI,0.81to 1.32])
Thiazide diuretic vs.placebo Mortality Low (69)No reduced risk (RR,1.17[CI,0.74to 1.85])Reduced risk for stroke NR
ESRD Insufficient
NA
Calcium-channel blocker vs.?-blocker
Mortality Low (46,67,68)No reduced risk (RR,0.62[CI,0.31to 1.22])
No reduced risk for other outcomes reported
NR
ESRD
Low (46,67)No reduced risk (RR,1.00[CI,0.70to 1.44])Calcium-channel blocker vs.diuretic Mortality Insufficient NA
No reduced risk for other outcomes reported NR
ESRD Low (47)No reduced risk (RR,0.90[CI,0.67to 1.21])
Strict vs.standard blood pressure control
Mortality Low (46,75,76,78)
No reduced risk (RR,0.86[CI,0.68to 1.09])
No reduced risk for other outcomes reported
NR
ESRD
Low (46,75,78)No reduced risk (RR,1.03[CI,0.77to 1.38])Statin vs.control Mortality High (29,79,81–87)Reduced risk (RR,0.81[CI,0.71to 0.94])
Reduced risk for MI,
stroke,most composite vascular outcomes reported
NR
ESRD
Low (79,80)No reduced risk (RR,0.98[CI,0.62to 1.56])
Low-protein diet https://www.doczj.com/doc/9a7059207.html,ual-protein diet
Mortality Low (93–96)No reduced risk (RR,0.58[CI,0.29to 1.16])
Reduced risk for composite renal outcome (1trial reporting)Weight loss,weight gain,hyperkalemia
ESRD
Low (92–94)No reduced risk (RR,1.62[CI,0.62to 4.21])Strict https://www.doczj.com/doc/9a7059207.html,ual glycemic Mortality Insufficient NA No reduced risk for other NR ACE ?angiotensin-converting enzyme;ARB ?angiotensin II–receptor blocker;CHF ?congestive heart failure;CKD ?chronic kidney disease;CVD ?cardiovascular disease;ESRD ?end-stage renal disease;MI ?myocardial infarction;NA ?not applicable;NR ?not reported;RCT ?randomized,controlled trial;RR ?relative risk.*Adverse events were sparsely reported in the trials included in this study and often similar in control and treatment groups.
?Data derived from a study comparing ACE inhibitor plus ARB combination therapy with either ARB or ACE inhibitor monotherapy.
Clinical Guideline
Screening,Monitoring,and Treatment of Stage 1to 3CKD
risk for ESRD(46,67)or all-cause mortality(46,67,68) compared with?-blocker monotherapy(Table3).No sta-tistically signi?cant difference in renal outcomes was reported.
Calcium-Channel Blockers Versus Diuretics.Low-quality evidence showed that calcium-channel blocker monotherapy did not statistically signi?cantly reduce the risk for ESRD compared with diuretic monotherapy(47) (Table3).Mortality data were not reported.There were no statistically signi?cant differences in renal or vascular outcomes reported.
Thiazide Diuretics Versus Placebo.No renal outcomes were reported for the comparison of thiazide diuretic monotherapy with placebo.Low-quality evidence showed no difference between the2groups in risk for all-cause mortality(69)(Table3).Diuretic monotherapy statisti-cally signi?cantly reduced the risk for stroke and1com-posite vascular outcome.
Combination Therapy Versus Monotherapy
ACE Inhibitors Plus ARBs Versus ACE Inhibitors Alone.Low-quality evidence showed no statistically sig-ni?cant difference in risk for ESRD between treatment with ACE inhibitors plus ARBs compared with ACE in-hibitors alone(70)(Table3).Moderate-quality evidence also showed no statistically signi?cant difference in the risk for all-cause mortality in the combined treatment group compared with monotherapy(50,71,72)(Table3).
ACE Inhibitors Plus ARBs Versus ARBs Alone.There was no evidence directly comparing the risk for ESRD or mortality with ACE inhibitors plus ARBs compared with ARB monotherapy.However,1trial(60)compared ACE inhibitor plus ARB combination therapy with either ARB or ACE inhibitor monotherapy(results for monotherapy reported together);moderate-quality evidence showed no reduced risk for ESRD,and low-quality evidence showed no reduced risk for all-cause mortality in the combined treatment group(Table3).
Other Comparisons.Evidence was insuf?cient to de-termine the effect of the following comparisons on ESRD or mortality:ACE inhibitors plus calcium-channel blockers versus ACE inhibitor monotherapy or calcium-channel blocker monotherapy;ACE inhibitors plus diuretics versus ACE inhibitor monotherapy;and ACE inhibitors plus di-uretics versus placebo.
Combination Therapy Versus Combination Therapy
Evidence was insuf?cient to determine the effect of the following comparisons on ESRD or mortality:ACE inhib-itor plus ARB versus ACE inhibitor plus aldosterone an-tagonist;ACE inhibitor plus diuretic versus ACE inhibitor plus calcium-channel blocker;ACE inhibitor plus aldoste-rone antagonist versus ACE inhibitor plus placebo;and ACE inhibitor and ARB plus aldosterone antagonist versus ACE inhibitor and ARB plus placebo.Strict Versus Standard Blood Pressure Control
Seven studies(46,73–78)randomly assigned patients with stage1to3CKD(mostly with hypertension)to strict versus standard blood pressure targets,and medications varied among studies.The mean achieved blood pressure ranged from128to133mm Hg systolic and75to81mm Hg diastolic in the strict-control group versus134to141 mm Hg systolic and81to87mm Hg diastolic in the standard-control group.Low-quality evidence showed no difference in risk for ESRD(46,75,78)or all-cause mor-tality(46,75,77,78).between strict and standard blood pressure control(Table3).There was no statistically sig-ni?cant difference between other reported vascular or renal outcomes.
Non–Blood Pressure Control Interventions
Statins Versus Control
Low-quality evidence showed that treatment with statins(3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors)did not reduce the risk for ESRD in patients with dyslipidemia and stage1to3CKD(79,80)(Table 3).Moderate-quality evidence(subgroup analyses)showed that statins reduced the risk for all-cause mortality in pa-tients with dyslipidemia as well as stage1to3CKD(RR, 0.81[CI,0.71to0.94])(29,79,81–87).Statins were found to statistically signi?cantly reduce the risk for MI, stroke,and most composite vascular outcomes reported.
Low-quality evidence from1trial(88)that reported on mortality in patients with CKD and dyslipidemia treated with high-dose atorvastatin(80mg/d)versus low-dose atorvastatin(10mg/d)found no difference in the risk for all-cause mortality(7.0%vs.7.5%,respectively;RR 0.93[CI,0.72to1.20]);however,the high-dose atorvasta-tin group had a decreased risk for CHF hospitalization and composite vascular outcomes.Another study(89)reported no differences between high-and low-dose statin treatment in terms of composite vascular outcomes.No results were reported for ESRD or any renal outcomes.
Gem?brozil Versus Placebo or Control
Low-quality evidence from a single trial(90)supports no difference in all-cause mortality reduction for treatment with the triglyceride-lowering medication gem?brozil com-pared with placebo(RR,0.91[CI,0.52to1.62]).No individuals in the study experienced ESRD.Gem?brozil was found to statistically signi?cantly reduce the risk for the composite outcome of fatal coronary heart disease, nonfatal MI,or stroke compared with placebo.Evidence was insuf?cient to determine whether treatment with gem-?brozil reduced the risk for ESRD or all-cause mortality compared with a triglyceride-lowering diet(91).
Low-Protein Diet Versus Usual-Protein Diet
Low-quality evidence from3trials comparing a low-protein diet with usual diet in patients with stage1to3 CKD(92–94)showed no statistically signi?cant difference
Clinical Guideline Screening,Monitoring,and Treatment of Stage1to3CKD
in association with ESRD(Table3),and data from4trials (93–96)showed no statistically signi?cant difference in the risk for all-cause mortality(Table3).
Intensive Diabetes Control Versus Usual Care
Evidence was insuf?cient to determine whether inten-sive glycemic control in patients with type1or type2 diabetes improved the risk for ESRD or all-cause mortality. Intensive Multicomponent Treatment Versus Usual Care Low-quality evidence showed no reduced risk in ESRD(97–100)or all-cause mortality(97–101)between the intensive multicomponent treatment and usual care (Table3).
H ARMS OF T REATMENT S TRATEGIES FOR S TAGE
1TO3CKD
Most of the trials did not report adverse events,and those reported were similar for patients with CKD and other patients treated with the same drugs.The most com-monly reported adverse event with ACE inhibitor treat-ment was cough.Therapy with ARBs was associated with statistically signi?cantly increased hyperkalemia(3.2%vs.
1.3%with placebo;RR,
2.38[CI,1.57to
3.61]).Adverse events associated with?-blocker therapy included heart failure,fatigue,bradycardia,dizziness,and hypotension. One trial(60)reported that ACE inhibitor plus ARB was associated with statistically signi?cantly increased risk for cough,hyperkalemia,hypotension,and acute kidney fail-ure requiring dialysis(RR,1.95[CI,1.09to3.49])com-pared with ACE inhibitor monotherapy.No adverse events were reported for other therapies included in the review. S UMMARY
No randomized,controlled trials evaluated the bene?ts and harms of screening for stage1to3CKD.Bene?t of screening would be derived from the anticipated bene?ts of treatment.No studies tested the sensitivity and speci?city of1-time screening in the general population using esti-mated GFR or albuminuria for diagnosis of CKD.There was no evidence evaluating the bene?ts of early treatment on clinical outcomes of patients with CKD who were iden-ti?ed through screening.Potential harms of screening in-clude labeling,adverse effects of unnecessary tests and treatments,and?nancial rami?cations.
No randomized,controlled trials evaluated the bene?ts and harms of monitoring patients with stage1to3CKD for disease progression.Rates of annual GFR decline vary, and lower GFR rates have been associated with increased mortality risk.Because there is considerable individual variability in albuminuria measurements,there are con-cerns about the accuracy of longitudinal measurement for CKD progression.Also,evidence evaluating the validity and reliability of the monitoring tests is lacking.Potential harms of monitoring for CKD progression are the same as
those for screening.
Many patients,regardless of CKD status,are already
taking ACE inhibitors,ARBs,statins,or other drugs to
treat existing comorbid conditions.Monotherapy with
ACE inhibitors or ARBs statistically signi?cantly reduced
the risk for ESRD in patients with CKD,but bene?ts were
limited to patients with macroalbuminuria,and most of
these patients also had diabetes and hypertension.No stud-
ies showed that treatment with other drug monotherapy
statistically signi?cantly reduced the risk for ESRD.Treat-
ment with statins reduced the risk for mortality,MI,and
stroke in patients with hyperlipidemia.?-Blocker therapy also reduced the risk for mortality,MI,and CHF,al-
though most of the patients included in the studies were
already being treated with ACE inhibitors or ARBs.
Calcium-channel blockers,diuretics,a low-protein diet,in-
tensive diabetes control,and intensive multicomponent in-
terventions did not reduce the risk for ESRD or all-cause
mortality compared with placebo or control.
None of the combination therapies were shown to
have a bene?cial effect on reducing the risk for ESRD or
all-cause mortality compared with monotherapy.Evidence
was insuf?cient to determine the ef?cacy of various com-
bination therapies compared with other combination ther-
apies for reducing risk for ESRD or all-cause mortality.
Harms of pharmacologic treatments were not gener-
ally reported speci?cally for patients with patients and were
similar to adverse effects experienced by all other patients
treated with the same drug(Table3).
The Figure summarizes the recommendations.
R ECOMMENDATIONS
Recommendation1:ACP recommends against screening
for chronic kidney disease in asymptomatic adults without risk
factors for chronic kidney disease.(Grade:weak recommenda-
tion,low-quality evidence)
Screening is recommended when it improves impor-
tant clinical outcomes while limiting harms for screened
individuals.Screening for CKD does not meet these gen-
erally accepted criteria for population-based screening
(102).Although prevalence increases with age,CKD has a
relatively low prevalence in the general population without
risk factors.The accuracy of available screening measures
for CKD or its progression is uncertain.No available evi-
dence evaluates the sensitivity and speci?city of various
screening tests in the general population.Albuminuria and
serum creatinine-derived estimated GFR are widely avail-
able in primary care settings,with a high sensitivity and
high speci?city for1-time measures of renal damage or
dysfunction,but the risk for false-positive results is also
very high(5,103,104).
There was no evidence evaluating the bene?ts of early
treatment in patients identi?ed by screening.In contrast,
harms,including false-positive results,disease labeling,and
Clinical Guideline
Screening,Monitoring,and Treatment of Stage1to3CKD
Clinical Guideline Screening,Monitoring,and Treatment of Stage1to3CKD
ACE?angiotensin-converting enzyme;ARB?angiotensin II–receptor blocker;CKD?chronic kidney disease;ESRD?end-stage renal disease; GFR?glomerular?ltration rate.
unnecessary testing and treatment,are associated with the screening.Given the potential harms of screening for stage 1to3CKD and unknown bene?ts,current evidence does not support screening for stage1to3CKD in adults with-out risk factors.
Recommendation2:ACP recommends against testing for proteinuria in adults with or without diabetes who are cur-rently taking an angiotensin-converting enzyme inhibitor or an angiotensin II–receptor blocker.(Grade:weak recommen-dation,low-quality evidence)
Evidence suggests that treatment with ACE inhibitors (moderate-quality evidence)or ARBs(high-quality evi-dence)reduces the risk for ESRD.Whether there are ad-ditional bene?ts of testing patients who are already taking ACE inhibitors or ARBs for proteinuria is unknown.Pro-teinuria is an intermediate marker;there is no evidence that monitoring proteinuria levels in patients taking ACE inhibitors or ARBs is bene?cial or that reduced proteinuria levels translate into improved outcomes for patients with CKD.
Recommendation3:ACP recommends that clinicians se-lect pharmacologic therapy that includes either an angiotensin-converting enzyme inhibitor(moderate-quality evidence)or an angiotensin II–receptor blocker(high-quality evidence)in patients with hypertension and stage1to3chronic kidney disease.(Grade:strong recommendation)
Evidence showed that treatment with ACE inhibitors (moderate-quality)or ARBs(high-quality)reduces the risk for ESRD in patients with stage1to3CKD.These med-ications also reduced composite renal outcomes,the risk for doubling of serum creatinine,and the progression from microalbuminuria to macroalbuminuria.Head-to-head tri-als revealed no difference in outcomes with ACE inhibitors or ARBs.The harms of ACE inhibitors include cough, angioedema,hyperkalemia,rash,loss of taste,and leukope-nia.The harms of ARBs include hyperkalemia,angio-edema,and dizziness.
The current evidence did not show any bene?t of combination therapy with an ACE inhibitor plus an ARB compared with monotherapy with ACE inhibitors or ARBs.In addition,the risk for adverse effects signi?cantly increased with ACE inhibitor plus ARB combination ther-apy,including cough,hyperkalemia,hypotension,and acute kidney failure requiring dialysis.
Evidence revealed no difference in ESRD or mortality between strict blood pressure control(128to133/75to 81mm Hg)and standard control(134to141/81to 87mm Hg).
Recommendation4:ACP recommends that clinicians choose statin therapy to manage elevated low-density lipopro-tein in patients with stage1to3chronic kidney disease. (Grade:strong recommendation,moderate-quality evidence) High-quality evidence showed that statins reduced the risk for all-cause mortality.Evidence also showed that statins lower the risk for MI,stroke,and most cardiovas-cular outcomes in patients with stage1to3CKD.Patients included in the studies had mean low-density lipoprotein levels of142mg/dL(range,109to192mg/dL).
Two recently published systematic reviews not in-cluded in the AHRQ report also showed bene?ts of lipid-lowering therapy or statin therapy in patients with CKD (105,106).One study showed that statin therapy de-creased mortality and cardiovascular events in patients with stage1to3CKD(105),and the other study showed that lipid-lowering therapy(including statins)decreased cardiac death and atherosclerosis-mediated cardiovascular events in patients with CKD(106).Low-quality evidence showed no effect on the risk for ESRD in patients with stage1to 3CKD.
I NCONCLUSIVE A REAS OF E VIDENCE
Screening for CKD in Asymptomatic Adults With
Risk Factors
Although there are known risk factors for CKD(dia-betes,hypertension,and cardiovascular disease),ACP found the current evidence insuf?cient to evaluate the ben-e?ts and harms of screening for CKD in asymptomatic adults with CKD risk factors.
Periodic Monitoring of Patients Diagnosed With Stage
1to3CKD
No randomized,controlled trials evaluated the bene?ts and harms of monitoring patients with stage1to3CKD. There is a lack of evidence that modifying treatment when progression occurs improves patient outcomes.Harms also include adverse effects from follow-up tests,unnecessary testing,increased medical visits,and health care costs. Hence,ACP concluded there is no net bene?t of routinely monitoring patients with stage1to3CKD,although in-dividual monitoring could be helpful for some patients on the basis of their risk level.Examples of individual moni-toring include1)GFR to monitor progression of the dis-ease,changes in functioning,or well-being over time;2) monitoring blood pressure as both a cause and complica-tion of CKD;3)monitoring proteinuria and serum creat-inine;and4)monitoring pharmacologic medications. ACP H IGH-V ALUE C ARE A DVICE
The ACP found no evidence that screening for CKD in adults without risk factors improves clinical outcomes. In addition,there is no proven bene?t of screening adults who are already taking ACE inhibitors or ARBs for mi-croalbuminuria.In the absence of evidence that screening improves clinical outcomes,testing will add costs,owing to both the screening test and to additional follow-up tests (including those resulting from false-positive?ndings),in-creased medical visits,and costs of keeping or obtaining health insurance.
From the American College of Physicians,Philadelphia,Pennsylvania; University of Arkansas for Medical Sciences,Little Rock,Arkansas;The University of Kansas School of Medicine–Wichita,Wichita,Kansas;and
Clinical Guideline
Screening,Monitoring,and Treatment of Stage1to3CKD
West Los Angeles Veterans Affairs Medical Center,Los Angeles, California.
Note:Clinical practice guidelines are“guides”only and may not apply to all patients and all clinical situations.Thus,they are not intended to override clinicians’judgment.All ACP clinical practice guidelines are considered automatically withdrawn or invalid5years after publication, or once an update has been issued.
Disclaimer:The authors of this article are responsible for its contents, including any clinical or treatment recommendations.No statement in this article should be construed as an of?cial position of the Department of Veterans Affairs.
Financial Support:Financial support for the development of this guide-line comes exclusively from the ACP operating budget.
Potential Conflicts of Interest:Dr.Shekelle:Personal fees:ECRI Insti-tute,Veterans Affairs,UptoDate;Grants:Agency for Healthcare Re-search and Quality,Veterans Affairs,Centers for Medicare&Medicaid Services,Of?ce of the National Coordinator for Health Information Technology.All other authors have no disclosures.Disclosures can also be viewed at https://www.doczj.com/doc/9a7059207.html,/authors/icmje/Con?ictOfInterestForms .do?msNum?M12-3186.A record of con?icts of interest is kept for each Clinical Guidelines Committee meeting and conference call and can be viewed at https://www.doczj.com/doc/9a7059207.html,/clinical_information/guidelines/guidelines/ con?icts_cgc.htm.
Requests for Single Reprints:Amir Qaseem,MD,PhD,MHA,Amer-ican College of Physicians,190N.Independence Mall West,Philadel-phia,PA19106:e-mail,aqaseem@https://www.doczj.com/doc/9a7059207.html,.
Current author addresses and author contributions are available at www https://www.doczj.com/doc/9a7059207.html,.
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Clinical Guideline Screening,Monitoring,and Treatment of Stage1to3CKD
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In the Clinic is a monthly feature in Annals that focuses on practical management of patients with common clinical conditions.It offers evidence-based answers to frequently asked questions about screening,prevention,diagnosis,therapy,and patient education and provides phy-sicians with tools to improve the quality of care.In the Clinic includes links to ACP Smart Medicine and CME quizzes offering category 1CME credit.
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Clinical Guideline
Screening,Monitoring,and Treatment of Stage 1to 3CKD
Current Author Addresses:Drs.Qaseem and Starkey:American Col-lege of Physicians,190N.Independence Mall West,Philadelphia,PA 19106.
Dr.Hopkins:University of Arkansas for Medical Sciences,4301West Markham Street,Little Rock,AK72205.
Dr.Sweet:The University of Kansas School of Medicine–Wichita,1010 North Kansas,Wichita,KS67214.
Dr.Shekelle:West Los Angeles Veterans Affairs Medical Center,11301 Wilshire Boulevard,Los Angeles,CA90073.Author Contributions:Conception and design: A.Qaseem,R.H. Hopkins,D.E.Sweet,P.Shekelle.
Analysis and interpretation of the data:A.Qaseem,R.H.Hopkins, M.Starkey.
Drafting of the article:A.Qaseem,R.H.Hopkins,D.E.Sweet,M. Starkey.
Critical revision for important intellectual content: A.Qaseem, R.H.Hopkins,M.Starkey,P.Shekelle.
Final approval of the article:A.Qaseem,R.H.Hopkins,D.E.Sweet, P.Shekelle.
Statistical expertise:A.Qaseem.
Administrative,technical,or logistic support:A.Qaseem,M.Starkey. Collection and assembly of data:A.Qaseem,R.H.Hopkins.
Annals of Internal Medicine
境外肿瘤护理发展对我国的启示 泰山医学院护理学院刘化侠 随着肿瘤学的发展，肿瘤护理已成为一门专门的护理学科。1976年英国RoyalMorsden肿瘤专科医院和美国Sloan一KaHering癌症医院，为加强国际间肿瘤专科护理的协作，会聚于伦敦，决定由Sloan一KaHering医院出版癌症护理杂志，由RogalMarsden医院组织召开国际肿瘤护理会议。1978年，《癌症护理》杂志正式出刊，同年在伦敦召开了第一届国际肿瘤护理会议，以后每两年举行一次。以上这两件大事推动了肿瘤护理事业的发展，不少国家相继建立了自己的肿瘤护理组织。 随着癌症成为全球的公共卫生问题，肿瘤护理逐渐发展为一门学科。在20世纪70年代在美国发展，首先出版杂志《肿瘤护理论坛》，之后86年出版《cancer nursing》(肿瘤护理) 1.境外肿瘤护理的发展史 。国际肿瘤护士协会(IsNCC)于1984年成立。它的基本任务是推动和发展国际肿瘤事业;传播肿瘤理论与知识，组织召开国际肿瘤护理会议;出版杂志、通讯，促进信息交流;与其它国际组织密切协作，提供咨询。本协会主席RobertTiffany 被聘请为UICC和WHO的专家组的成员，1989年又荣任国际护士会理事。国际肿瘤护士协会的理事会由21名理事组成，按世界自然区划分，欧洲、北美、中南美洲，中东和非洲，运车和澳洲等五大区各设三名理事。1988年，我国护士代表被推选为理事。早在七十年代，国际抗癌联盟(UICC)与美国抗癌协会(ASC)合作，为不少国家培训了肿瘤专科护士。1978和1980年，UICC和wHO与国际护士会(ICN)两次举行会议，制定肿瘤护理教育计划，并明确护士在肿瘤防治中的作用。UICC每四年举行的国际肿瘤会议，过去没有护士参加。1978年第12届会议在布谊诺斯艾利斯举行，在会议主席Abalcanonico博士倡导下，第一次邀请护士参加。1982年护士代表第一次在第13届会议上报告论文，阐明了对癌症实施“整体护理”的发展方向。 1.1 美国：美国癌症护理协会 肿瘤护理专业发展概况
慢性肾脏病（CKD）定义、诊断及分期慢性肾脏病(CKD)定义、诊断及分期 ——KDIGO伦敦研讨会纪要 2009年10月4-6日，慢性肾脏病:改善全球预后(KDIGO)国际机构在英国伦敦召开了慢性肾脏病(CKD)定义、诊断及分期研讨会。其主要目的是汇总全球CKD随访资料，以预后为硬终点，评价估算的肾小球滤过率(eGFR)及尿白蛋白与终点事件间关系，对现行CKD诊断和分期系统进行重新评估。 来自全球十余个国家和地区的近百位肾脏及全科医师，检验医学、流行病学、统计学专家和社区卫生保健者代表出席了本次会议，这其中既有现行CKD诊断系统的制定和拥护者，也有持不同观点的专家和学者。 唯一受邀参加此次高端学术研讨会的中国大陆学者、北京大学第一医院王海燕教授和王芳医师对此次会议的背景及所获部分成果等内容进行了系统介绍，希望对我国临床医师有所助益。 背景 2002年，美国肾脏病学会(ASN)制定的肾脏病/透析临床实践指南(KDOQI)提出了CKD诊断的全新概念，用以代替既往的“慢性肾损伤”、“慢性肾衰竭”等名称，并制定了分期系统(见右表)。 表2002年KDOQI的CKD分期系统 分期描述根据严重度分类根据治疗分类 肾损伤伴GFR正常GFR?90 T代表移植 1 或升高 肾损伤伴GFR轻度GFR为60~89 2 下降
GFR中度下降 GFR为30~59 3 GFR严重下降 GFR为15~29 4 肾衰竭 GFR<15(或透析) D代表透析 5 注:GFR肾小球滤过率，单位为ml/(min?1.73m2) 2004年，国际肾脏病学会(ISN)的KDIGO采纳了CKD的定义和分期系统并向全球推广，使其分别成为全球肾脏病相关医疗及学术交流的统一疾病分类名词和划分标准。 7年来，CKD领域的新研究不断涌现，尤其是在普通和高危人群中进行的早期CKD流行病学调查，如欧美、我国等全球多个国家和地区均进行了CKD筛查研究。与2000年相比，目前在Pubmed上可检索到的CKD相关文献已增加1倍以上。肾脏早期评估计划(KEEP)、肾脏和血管终末期疾病预防(PREVEND)等多个CKD随访人群的建立，将有利于进一步明确CKD危险因素和防治措施。 CKD流行病学研究的开展，唤起了公众和非肾脏病专科医师对CKD的关注，提高了CKD是公共卫生问题的意识，推动了CKD公共卫生政策的制定，获得了相当的社会效应。 问题 虽然2002年的CKD定义及分期系统堪称CKD发展史上的里程碑，但由于受到当时循证医学证据的限制，仍可能存在不足。随着近年来相关证据的不断积累，对该系统的质疑和争论日益凸显，是否应对其进行修订也被提上日程。 过度诊断, 以KDOQI的CKD定义及分期为依据的流行病学调查显示，CKD的人群患病率为6%,16%，这一比率远高于肾内科医师的日常接诊量，且与终末期肾脏病(ESRD)患者的实际数量亦不成比例;此外，新增的CKD人群主要集中于CKD3期，且以老年人多见。上述结果引发了是否由于CKD的定义导致其患病率被高估的质
美国癌症协会(ACS)公布防癌指南 2015-01-15林烁Nathan 美国癌症协会(ACS)每5年要发布一期关于饮食、营养和体育运动与癌症预防之间关系的报告，作为对大众的科学知识普及、各卫生健康机构和社区团体之间的交流和有关政策方针制定的指南.现摘要公布2010年ACS防癌指南. 1.乳腺癌：美国妇女最多见的肿瘤，为妇女第二大死亡原因的癌症，仅次于肺癌。绝经后妇女体重超重，则患乳腺癌的风险显著增加。这与过多脂肪导致血内雌激素水平过高有关。过多饮酒并叶酸摄入不足也会增加乳腺癌发生的风险。体育锻炼可降低这一风险。 2.结、直肠癌：在美国因癌症死亡总人数中居于第2位。肥胖与其有直接关系，男性尤其显著。大量摄入蔬菜水果和含粗纤维谷物，减少红肉及加工肉类食品的摄入，适当摄入维生素D和钙，同时加强日常的体育锻炼可以降低其发生的风险。另外，定期筛检、及时发现和切除肠道腺瘤(癌前病变)也至关重要。 3.肺癌：美国因癌症死亡的第一大因素。超过85％的患者发病与烟草有关。戒烟和大量摄入蔬菜水果有助于降低其发生。但要注意：过量食用含胡萝卜素和维生素A的保健食品反而会使吸烟者的肺癌发生危险系数升高。 4.子宫内膜癌：美国妇女癌症发病率中居第4位。子宫内膜癌与雌激素水平有关。通过大量运动，增加蔬菜、水果、粗纤维食品及豆类的摄入，保持健康体重均可降低其发生的可能性。 5.肾癌：占男性癌症发病及死亡的3％、女性的2％。直接相关因素有肥胖和吸烟。因此，戒烟及保持健康体重尤为重要。 6.胰腺癌：美国癌症死亡原因的第4位。吸烟、2型糖尿病、过多食用红肉及体育运动不足与其极为相关。 7.上呼吸道和消化道癌症：酗酒、吸烟显著增加口腔癌、咽喉癌和食管癌的可能。饮食过热导致食道灼伤，可引发食管的慢性炎症最终恶化为食管癌。改变不良饮食习惯，戒烟酒，减轻体重和多食新鲜蔬菜及水果有利于降低其发生的风险。
美国心脏病学会和美国心脏协会成人降胆固醇治疗指南 美国心脏病学会(ACC)与美国心脏协会(AHA)联合颁布了成人降胆固醇治疗降低动脉粥样硬化性心血管疾病(ASCVD)风险指南[1]。该指南以现有研究证据为依据，强调他汀类药物在降低ASCVD风险方面的获益，对ASCVD的一级、二级预防及风险评估、他汀类药物的管理、药物不良反应的处理等方面提出了具体建议。这一指南虽然针对西方人群所制定，但对我国人群的血脂异常管理与ASCVD的防治具有很好的参考价值。现将其要点介绍如下。 1 指南要点 1.1 强调他汀类药物降胆固醇可降低ASCVD风险 指南以多项随机对照试验研究结果为依据，明确以下4组患者可由他汀类药物治疗获益：(1)确诊ASCVD者；(2)原发性低密度脂蛋白胆固醇(LDL-C)升高(≥4.9 mmol/L)；(3)40～75岁、LDL-C为1.8～4.9 mmol/L 的糖尿病患者；(4)无ASCVD与糖尿病，但其10年ASCVD风险≥7.5%者。指南重点强调他汀类药物在ASCVD一级和二级预防中降低ASCVD 风险的重要作用，并对其治疗强度作出了分级推荐(表1)。 表1
不同剂量他汀类药物的降胆固醇幅度 1.2 LDL-C和(或)非高密度脂蛋白胆固醇(non-HDL-C)治疗目标值缺乏证据 专家组认为目前没有证据支持为不同人群制定相应的LDL-C和(或)non-HDL-C治疗目标。在ASCVD常规预防措施中，对最可能获益人群应用适当强度的他汀类药物治疗可降低ASCVD风险。非他汀类药物治疗的获益/风险比尚待明确。 1.3 更新他汀类药物一级预防风险评估 指南推荐对所有患者评估其10年ASCVD风险，并确定他汀类药物治疗最能获益的对象。启动他汀类药物治疗之前，医生与患者要充分沟通。 1.4 药物安全性建议 多项随机对照试验提示要充分考虑用药安全性问题。指南强调重视他汀类药物不良反应，并为包括肌溶解等在内的不良反应的处理提供临床指导。 1.5 生物标记物与无创性检测的作用 对于不属于上述4组他汀类药物获益人群的患者，可进行相关生物标记物与无创检测，以为风险评估提供更多依据。 2 他汀类药物的应用建议 2.1 ASCVD患者二级预防 临床已诊断ASCVD的患者，若年龄≤75岁，且无用药禁忌，无论性别，均应启动并长期服用大剂量他汀类药物治疗(ⅠA)。若患者不能耐受强效他汀类药物治疗或出现他汀类药物相关性不良反应，可尝试中等强度他
For personal use only in study and research; not for commercial use 薄慢性肾衰竭 ( 附慢性肾脏病诊疗指南芄【概述】肁慢性肾衰竭(chronic renal failure ，CRF) 是指慢性肾脏病引起的肾小球滤过率 蝿( glomerular filtration rate, GFR )下降及与此相关的代谢紊乱和临床症状组成的综合蚆征，简称慢性肾衰。 莂慢性肾衰可分为以下四个阶段:(1)肾功能代偿期；(2)肾功能失代偿期；(3)肾功能衰竭蒁期(尿毒症前期)；(4)尿毒症期(表48-1) 。 蒀表48-1 我国CRF 的分期方法(根据1992 年黄山会议纪要) 蚇CRF分期肌酐清除率(Cer)血肌酐(Ser)说明 螄205 羀(ml∕min)( μ mol∕l) (mg∕dl) 芀肾功能代偿期50 ?80 133 ?177 1.5 ?2.0大致相当于CKD2 期 蒄肾功能失代偿期 20? 50 186?442 2.1?5.0 大致相当于CKD3 期 袃肾功能衰竭期10?20451 ? 707 5.1?7.9大致相当于CKD4 期 莀尿毒症期<10≥707≥8.0大致相当于CKD5 期 羁注：肌酐分子量为113，血肌酐的单位互换系数为0.0113 或88.5。 薆如: 1.5 mg∕dl=1.5 × 88.5= 132.75 μ mol∕l ≈133μ mol∕l 或1.5÷ 0.0113=132.74 μ mol∕l 膅≈ 133 μ mol/l 肃晚近美国肾脏病基金会K∕DOQI 专家组对慢性肾脏病(ehronie kidney d iseases ，CKD) 蒇的分期方法提出了新的建议（见附录: 慢性肾脏病）。显然，CKD 和CRF 的含义上有相当大的 蚇重叠，前者范围更广，而后者则主要代表CKD 患者中的GFR 下降的那一部分群体。
美国心脏病学会(ACC)和美国心脏协会(AHA)《美国高血压临床实践指 南》（二） 美国当地时间11月13日，由美国心脏病学会(ACC)和美国心脏协会(AHA)联合多个学术机构共同制定的美国新版高血压指南正式颁布。中国医师协会高血压专业委员会（CHC）组织专家进行了一次线上专家研讨会（查看解读一）。 全国各地的高委会专家第一时间研究了美国2017高血压临床实践指南的内容，并结合中国的高血压指南以及中国临床实践的实际情况进行了深入的探讨和交流。本期评述专家为：名誉主委孙宁玲教授、副主委李玉明教授、副主委杨天伦教授、委员张新军教授，分别对指南进行了述评。 名誉主委孙宁玲教授 诊断高血压指南的标准前移，即≥130/80 mmHg 基于美国10年来（2007－2017年）高血压的患病人数增加13.7％，接受药物治疗的仅增加了1.9％（34.2％~36.2％/10年）这样一个特点，同时也基于一些重要的研究，例如SPRINT研究和JAMA的meta分析，
鉴于美国患病人数与治疗人数之间存在的巨大差别。诊断目标的前移，以及早期血压管理对美国改善高血压所导致的器官损害和疾病具有一定的意义。 药物治疗理念 以10年风险＞10％+ 血压≥130/80 mmHg可以启动降压药物的治疗，而前面任何一种状况（仅10年风险＞10％或者血压≥130/80 mmHg且＜140/90 mmHg）都是以强化的生活方式干预为主的治疗，而不必强调药物治疗。 我们最关心的问题还是：美国指南的这种血压分级理念和治疗理念适合中国吗？ 以下几个问题需要思考： （1）要看中国目前有多少血压在≥130/80~140/90 mmHg的人群（2）在这样的人群中，10年心血管风险＞10％的有多少？ （3）目前的我国的生话方式干预的结果可以使多少人达到血压下降5％~10％的效果 （4）中国目前心血管危险因素（血压、血脂）和心脑血管疾病（冠心病、脑卒中）的直接线性关系是什么？血压高直接导致脑卒中的风险升
美国心脏病学会/美国心脏病协会关于心电图及动态心电图 的临床能力评估 Ⅰ.绪言 内科医生的临床工作权限许可是医疗机构维护卫生质量的基本机制。卫生组织授权联合委员会要求连续的临床工作人员权限许可,以申请者的评估为基础而非医学工作细则中的专业标准。内科医生自身也负责确认构成专业能力的标准及相应地评估其同事的工作。但是，对内科医生的知识与能力的评估过程通常受限于评估者自身的知识及汲取正确信息的能力，由于需要权限许可的高度专业操作的不断涌现，这些问题变得更加复杂了。 ACC/AHA/AIP/ASIM关于临床能力的工作组成立于1998年，致力于形成建议,这些建议为实现和维持特定心血管设备、操作或技术的充分应用提供必要的认识性的和技术性的技能。这些文件是以证据为基础的，如果没有证据，则专家的意见用于形成建议。 这些文件不包含特定设备的适应证或禁忌证。建议用于帮助那些判断心血管卫生关怀提供者能力的人，这些提供者包括初次执业者和（或）已执业者及经历定期专业性检验审查的执业者。能力评估是复杂和多方面的，所以单一建议并不是完备的或适合于判定所有能力。 ACC/AHA/AIP-ASIM工作组尽其努力避免任何现存的或潜在利益冲突，这些利益冲突可能由外部关系或ACC/AHA写作委员会成员的个人利益引起，尤其是所有写作委员会成员被要求提供各种与现实或潜在利益冲突的关系的公开评价。这些变化被写作委员会评估并且变化出现后会被刷新。 Ⅱ．引言 Ａ.委员会的组织和证据回顾 本文件是１９９５年ＡＣＰ／ＡＣＣ／ＡＨＡ心电学临床能力评估的修订版。写作委员会由２名ＡＣＣ及２名ＡＨＡ心电学知名专家组成，既代表学术部门也代表私人执业部门。文件由2名ACC提名的评估官员，3名AHA、ACC临床心电生理委员会、临床心脏病学委员会心电学和心律失常分会提名的评估官员，和写作委员会提名的16位具备资格的评审人员评估。2001年8月3日，由ACC评议委员会和AHA科学顾问及协作委员会批准出版。本文件是目前通行的，除非工作组修订或从分发中撤回。另外国际Holter 和无创心电学协会官方委员会也正式认可本文件。 B.临床能力评估的目的 该能力评估是ACC和AHA发展的一系列评估之一，用以评估内科医生在特定操作基础方面的能力。心电图和动态心电图的充分阅读与解释所需的最基本的教育、培训、经历及必要的有认识力的技术被具体说明。这些最基本的培训和经历的能力建议是在宽泛意上说的，这一点很重要。而对施行于患者的在少见诊断或标准操作的罕见变异的专业性检验，还要求另外的经历或培训。所以即使有较好能力的执业者偶而也会咨询有专业兴趣、经历或能
美国癌症协会公布9大防癌建议，其中有四个很多人忽略了！ 主要癌症预防干预措施，大概可以归类为9个方面： 控烟 限酒 控制肥胖 健康饮食 运动 预防病原体感染 防晒 减少不必要医用放射 减少室内材料污染 其中，预防病原体感染、防晒、减少医用放射、减少室内材料污染 4个方面往往被不少人忽略掉！ 结合我们自己的情况，一起来看看这些防癌建议： 1. 远离11种病原体 目前，共11种病原体被国际癌症研究机构（IARC）认定有致癌性，包括： ▼1种细菌：幽门螺旋杆菌；
▼7种病毒：乙肝病毒、丙肝病毒、人乳头状瘤病毒（HPV）、EB病毒、人类免疫缺陷病毒等。 ▼3种寄生虫：泰国肝吸虫、华支睾吸虫（肝吸虫）、埃及血吸虫。 对于一般生活中常见的感染，我们建议： ▍① 宫颈癌——HPV人体乳头状瘤病毒 途径：性传播途径、密切接触、间接接触(感染者的衣物、生活用品、用具等)、医源性感染、母婴传播。 预防：接种HPV疫苗、注意个人卫生、注意性生活卫生。有过性行为的女性，最好每年做一次筛查。 提醒：感染HPV早期无明显症状，引起宫颈病变后，可能出现性生活接触性出血、白带增多有异味、经期延长月经量增多等，要及时就医。 ▍② 胃癌——幽门螺旋杆菌 途径：口腔唾液、粪便经手、食物接触口 预防：餐前要洗手，尽量不要喂送食物，尤其不要口口喂养幼儿。可以分餐制或公筷，且餐具经常消毒。 提醒：如果出现口臭、泛酸、胃痛等症状的患者，应做胃镜和hp感染筛查。 ▍③ 肝癌——乙肝和丙肝病毒、肝吸虫 途径：血液传播、母婴传播、性传播、生吃淡水
鱼虾等 预防：接种乙肝丙肝疫苗；在献血或输血时去正规医疗机构；做好婚检孕检；少吃生的淡水鱼虾。 提醒：慢性乙肝、丙肝患者可能出现乏力、食欲不振、消化不良等症状，切不可轻视。 ▍④ 鼻咽癌——EB病毒 途径：唾液传播 预防：接种EB疫苗，注意避免口对口传播和喷嚏飞沫传播。 2. 防晒，减少皮肤癌风险 防晒是被不少人忽略的！然而，太阳紫外线辐射可导致皮肤黑色素瘤、鳞状细胞癌和基底细胞癌。比如Meta分析显示，10次晒黑设备暴露就可导致皮肤黑色素瘤风险增加34%。 晒太阳是补充维生素D的好方式，但我们拒绝暴晒！ 建议： ▍① 避免正午太阳直射； ▍② 适当使用防晒霜； ▍③ 戴宽沿遮阳帽和太阳镜； ▍④ 穿防晒衣； 3. 减少不必要医用放射
慢性肾衰竭诊疗指南 中华中医药学会 关键词：慢性肾衰竭；诊疗规范指南；关格；中医药疗法；中医标准化 慢性肾衰竭（chronicrenalfailure，CRF）是指发生在各种慢性肾脏疾病的基础上，肾实质遭到严重破坏，缓慢地出现肾功能减退直至衰竭。临床上以肾功能减退、代谢废物潴留、机体内环境失衡为主要表现，恶心呕吐是最突出的症状。本病属于中医学的“溺毒”、“虚劳”、“关格”等范畴。 1 诊断依据 1.1 临床表现 1.1.1 症状临床表现十分复杂，基本可以分为代谢紊乱和各系统症状两大组。但两者亦互为因果，许多代谢紊乱可以是系统症状的基本原因，反过来，各系统脏器因代谢异常而导致毒性代谢产物潴留，影响脏器功能，从而加剧代谢紊乱。 1.1.2 体征慢性肾衰竭患者无明显特异性的体征，主要根据患者的原发病及控制情况、肾功能损害、并发症、生活方式的调节等不同而表现各异，如水肿、高血压、皮肤改变等。 1.2 理化检查 1.2.1 尿常规检查可有程度不等的蛋白尿、血尿、管型尿，也可无明显尿检异常，以24h尿肌酐计算肌酐清除率，有明显下降。 1.2.2 血常规检查有红细胞、血红蛋白、红细胞压积的明显下降，部分患者可有白细胞和血小板的减少；肾功能有尿素氮及血肌酐的明显升高，达到失代偿指标；早期患者可呈低钙高磷，在合并甲状旁腺功能亢进时可呈高钙高磷，慢性肾功能不全患者应注意血钾水平的变化及酸中毒状态的纠正；血脂水平为甘油三酯的中度升高及胆固醇在不同脂蛋白的分布异常；血β2-微球水平可反映肾小球的滤过功能通常可升高，血碱性磷酸酶升高，钙磷乘积升高。病因诊断时述可以检查血糖、血尿酸、免疫指标等项目。 1.2.3 影像学检查包括B超、ECT、心脏超声、X线摄片等。 1.2.4 肾活检一般来说，慢性肾衰竭不是肾活检的适应证。 1.3 诊断要点参照中华内科杂志编委会肾脏病专业组1993年拟定标准制定。①内生肌酐清除率Ccr＜80ml／min；②血肌酐Scr＞133μmol／L；③有慢性肾脏疾病或累及肾脏的系统性疾病病史。 1.4 临床分期标准①肾功能不全代偿期：Ccr80～50ml／min，Scr＜1331μmol／L。 ②肾功能不全失代偿期：Ccr50～25ml／min，Scrl33～2211μmol／L。③肾功能衰竭期：Ccr25～l0ml／min，Scr221～4421μmol／L。④尿毒症期：Ccr＜10ml／min，Scr＞4421μmol／L。 2 辨证论治 本病为本虚标实，正虚为本，邪实为标；以正虚为纲，邪实为目。临床辨证分类以正虚为主，治疗多采用扶正与祛邪兼顾，标本同治。但应分清标本主次，轻重缓急。治本是根本措施，应贯穿在全过程中，治标可在某一阶段突出，时间宜短。因此，保护肾气和其他内脏
美国癌症联合委员会甲状腺癌分期系统（第8版）更新解读 孙威，贺亮，张浩 中国实用外科杂志2017,37(3):255-258 以肿瘤原发灶（T）、区域淋巴结转移（N）以及远隔转移（M）为基本组成的美国癌症联合委员会（American Joint Committee on Cancer，AJCC）甲状腺癌分期系统是目前世界范围内提供甲状腺癌预后信息，评估甲状腺癌预后分期重要的参考标准之一。AJCC第8版甲状腺癌分期系统与第7版相比，将分化型甲状腺癌分期所需的诊断年龄切点值从45岁增加至55岁；重新定义了T3分期及未分化癌的T分期；将Ⅶ区淋巴结转移从颈侧方淋巴结转移（N1b）划分至中央区淋巴结转移（N1a）；修改了分化型甲状腺癌、未分化癌TNM的分期。全新的TNM分期系统不仅对甲状腺癌的手术治疗具有重要的指导意义，还为病人的预后评估提供了重要的参考依据。 作者单位：中国医科大学附属第一医院甲状腺外科，辽宁沈阳110001 通信作者：张浩，E-mail：haozhang@https://www.doczj.com/doc/9a7059207.html, 以肿瘤原发灶（T）、区域淋巴结转移（N）以及远隔转移（M）为基本依据的美国肿瘤联合委员会（American Joint Committee on Cancer，AJCC）发行的甲状腺癌分期系统是目前世界范围内提供甲状腺癌预后信息，评估甲状腺癌预后分期重要的参考标准之一。其简单易行并且被美国甲状腺协会（ATA）和美国国立综合癌症网络(NCCN)甲状腺癌指南引用和推荐。AJCC第8版甲状腺癌分期系统的更新，将更精确的指导临床医生对病人进行临床和病理学分期，进而更精准的判定病人的预后，对规范甲状腺癌的诊治起到积极的促进作用。 1AJCC第8版甲状腺癌分期系统更新要点 AJCC第8版甲状腺癌分期系统延续采用以T、N、M为依据的解剖学分期原则，结合最新的甲状腺癌科学研究证据，主要对如下内容做出了相应修改。 将分化型甲状腺癌（differentiated thyroid cancer，DTC)预后所需的诊断年龄切点值从45岁增加至55岁。T分期部分：重新定义了T3分期，更改了未分化甲状腺癌（anaplastic thyroid cancer，ATC）的T分期。Ｎ分期部分：将Ⅶ区淋巴结转移从侧方淋巴结转移（N1b）更改为中央区淋巴结转移（N1a）。TNM分期部分：修改了DTC、ATC的TNM分期。甲状腺髓样癌作为一个新的
美国心脏病学会PAD诊疗指南概述 PAD是指除冠状动脉之外的主动脉及其分支动脉的狭窄、闭塞或瘤样扩张疾病. PAD后果严重,包括间歇性跛行、截肢、腹主动脉瘤破裂、严重的高血压和肾功能衰竭,心肌梗死(MI)、卒中和心性死亡发生率也增加。但病程进展隐匿,长时间可能没有临床症状,只有通过较为敏感的检查方法才能够检测出(如测量颈动脉内膜中层厚度),晚期才表现为肢体血压的变化和临床症状。 由于PAD临床症状不典型,临床医师在诊治患者时应注意询问和观察患者有无PAD表现。PAD表现包括行走时下肢无力或活动受限,足和腿部受伤后伤口不易愈合,直立或斜躺时局限于足或腿部的静息性疼痛,餐后腹痛伴有体重降低,直系亲属腹主动脉瘤病史。 体检时应注意:①患者双上肢血压是否对称,②颈动脉是否存在杂音,③腹部、腰胁部和股动脉处听诊是否有杂音,④估计腹主动脉的搏动和最大直径,⑤触摸肱动脉、挠动脉、尺动脉、股动脉、腘动脉、足背动脉和胫后动脉有无搏动异常,⑥采用Allen试验判断手部血流灌注,⑦检查足部皮肤的颜色、有无破溃和溃疡,⑧远端肢体的体毛消失、营养不良和指趾甲肥厚等表现支持患者存在严重PAD。 下肢PAD 1. 动脉粥样硬化是下肢PAD的主要原因。下肢PAD患者发生缺血性事件的危险增加。下肢PAD患者中仅10%~30%有间歇性跛行症状。大部分下肢PAD患者并没有可以被识别的肢体缺血症状,这部分人群可定义为无症状人群。虽然这部分患者没有典型症状,但是能够检测到动脉功能异常,发生心血管缺血性事件的风险增加。需要注意,无症状的下肢PAD患者的危险因素和有症状的下肢PAD患者相似。两组患者的糖尿病、吸烟史、高血压、高脂血症等的发生率都非常高,所以无论其症状是否典型,下肢PAD患者发生MI和缺血性卒中的危险明显增加。 对于无症状的下肢PAD患者的处理,目前没有证据表明血管的影像学检查手段,如节段压力测定、双功超声、磁共振血管成像(MRA)和血管造影,能够提供改善预后的附加信息。同样,对这些患者也没有证据表明血管成形术治疗能改善肢体的功能或缓解症状。没有典型间歇性跛行症状的下肢PAD患者应用药物治疗改善下肢功能作用的相对获益也没有证据。对这些患者应强调积极纠正危险因素,改善生活方式。如在高血压和高脂血症的指南中都将下肢PAD列为高危人群,无论有无症状,下肢PAD为冠心病的等危证,治疗目标是降低风险,各方面的治疗达标。 2. 虽然间歇性跛行或体检发现动脉搏动缺失或显著减弱提示下肢PAD,但 检查踝臂指数(ABI)常用于筛查下肢PAD。ABI<0.90诊断下肢PAD的敏感性为90%,特异性为95%。引起静息痛或溃疡的严重下肢PAD的ABI常小于0.40。 3. 下肢PAD的危险因素包括:年龄在50岁以下的糖尿病患者伴有一项其他的动脉粥样硬化危险因素,年龄在50~69岁之间有吸烟史或糖尿病,年龄在70岁以上,
解读美国临床肿瘤学会癌症患者静脉血栓栓塞防治指南癌症患者发生静脉血栓栓塞（VTE）的风险极高，并且早期死亡率高。由于药物的毒副作用及循证证据结果的多样化，因此针对这类人群有效安全的预防VTE面临巨大的挑战。2007年美国临床肿瘤学会颁布了最新关于癌症患者VTE的防治指南，进一步规范了癌症患者的抗凝治疗。（J Clin Oncol. 2007,25:5490） 癌症患者VTE的发生率高 VTE为癌症患者的主要并发症，发生率为4%~20%，并且可导致死亡。VTE包括深静脉血栓形成（DVT）及肺栓塞（PE）。癌症患者DVT的风险增加数倍，住院的癌症患者及正接受药物治疗的患者发生DVT的风险更大。基于人群的研究发现，癌症患者血栓形成的风险增加4.1倍，接受化疗的患者风险增加6.5倍。其实目前癌症患者VTE发生率（4%~20%）的报道远远低于尸解的发现，后者发生率为50%。 存在VTE的癌症患者死亡率高 一项回顾性观察研究提示，接受化疗的癌症患者，静脉和动脉血栓栓塞占死亡原因的9%。在发生VTE同时诊断癌症，或在发生VTE 1年内诊断的患者，1年时死亡率增加3倍。癌症患者接受外科手术，术后发生致命性PE的风险是接受同样手术非癌症患者的3倍。 癌症患者存在多个VTE危险因素 癌症患者发生VTE的危险因素因肿瘤的种类及自然病史的不同而异。恶性肿瘤诊断初期，VTE的风险最高。已有报道，某些部位的肿瘤，如胰腺、胃部、脑部、卵巢、肾脏、肺部肿瘤及已出现转移的肿瘤与VTE发生相关。最新研究提示，恶性血液系统疾病，特别是淋巴瘤与VTE发生显著相关。 接受活性药物治疗的癌症患者，VTE发生风险明显增加。使用新的抗肿瘤药物特别是抗血管再生的药物，VTE发生率较高。激素治疗特别是他莫西酚（tamoxifen）的应用及促红细胞刺激因子等可增加VTE的风险。癌症患者住院时VTE的风险明显增加。与非癌症患者相比，癌症患者接受外科手术，术后DVT风险增加2倍，致命性PE风险增加3倍。 其他可能的危险因素包括：化疗前血小板数量>350×109/L和存在致血栓的基因突变等（表1）。 表1 癌症患者VTE的危险因素 患者相关因素 高龄 种族 并存疾病（肥胖、感染、肾脏疾病、肺部疾病、动脉血栓栓塞） 既往VTE病史 化疗前血小板数量增加 遗传性致栓基因突变 肿瘤相关因素 原发肿瘤的部位（消化道、脑、肺、生殖系、肾脏、血液） 诊断后的最初3~6个月 肿瘤近期转移 治疗相关因素 近期接受大手术 正在住院 接受化疗 接受激素治疗 目前或近期接受抗血管再生治疗（thalidomide, lenalidomide）
2020美国癌症协会ACS2030年抗癌策略 美国癌症协会(ACS)发布了未来10年肿瘤一级抗击计划，称为“2030癌症预防和死亡率下降蓝图”，相关文章在全球影响因子最高期刊CA杂志上发表！ 80年，癌症死亡率下降26%！ 文章详细分析了1930~2010年这80年期间美国癌症死亡率改变和原因，为未来降低癌症死亡率的工作规划了方向。
上图是1930年到2015年80年间，美国男性和女性的癌症死亡率情况。可以看到，全美癌症死亡率最高的年份是1991年，这一年的总死亡率是215.1/10万人，而到2015年，全美癌症总死亡率已经降到158.7/10万人，降幅达到26%！ 国家在1988-90至2013-15期间乳腺癌死亡率下降。数据来源：美国国家卫生统计中心。
国家对1980 - 82年至2013 - 15年结肠直肠癌死亡率的下降。数据来源：国家卫生统计中心。 美国癌症协会：死亡率下降三大要素！ 癌症首先是预防，吸烟与否极大地影响了以肺癌为首的多种癌症，因此降低癌症死亡率靠戒烟。 其次是筛查，筛查的出现，极大地影响了结肠癌和宫颈癌的预后。虽然乳腺癌和前列腺癌筛查还有不同程度的争议，但还是有贡献的。 手术术式的改进和并发症的减少使得手术死亡率降低，放疗方法的进步降低了患者死亡率，同时针对血液系统和淋巴系统肿瘤的系统治疗进步也降低了死亡率。 未来十年10大抗癌策略！ 1远离11种病原体 一些病毒感染(如HPV、HIV和乙肝病毒)也会增加患癌症的风险。 目前，共11种病原体被国际癌症研究机构（IARC）认定有致癌性，包括： ?1种细菌：幽门螺旋杆菌； ?7种病毒：乙肝病毒、丙肝病毒、人乳头状瘤病毒（HPV）、EB病毒、人类免疫缺陷病毒等。 ?
慢性肾衰竭（附慢性肾脏病诊疗指南 【概述】 慢性肾衰竭(chronic renal failure，CRF) 是指慢性肾脏病引起的肾小球滤过率（glomerular filtration rate, GFR）下降及与此相关的代谢紊乱和临床症状组成的综合征，简称慢性肾衰。 慢性肾衰可分为以下四个阶段:(1)肾功能代偿期；(2)肾功能失代偿期；(3)肾功能衰竭 期(尿毒症前期)；(4)尿毒症期（表 48-1)。 表 48-1 我国 CRF 的分期方法（根据 1992 年黄山会议纪要） CRF 分期肌酐清除率(Ccr) 血肌酐(Scr) 说明 205 (ml/min) (μmol/l) (mg/dl) 肾功能代偿期 50～80 133～177 ～大致相当于 CKD2 期 肾功能失代偿期 20～50 186～442 ～大致相当于 CKD3 期 肾功能衰竭期 10～20 451～707 ～大致相当于 CKD4 期 尿毒症期 <10 ≥707 ≥大致相当于 CKD5 期 注：肌酐分子量为 113，血肌酐的单位互换系数为或。 如: mg/dl=×= μmol/l ≈ 133μmol/l或÷=μmol/l ≈ 133μmol/l 晚近美国肾脏病基金会 K/DOQI 专家组对慢性肾脏病(chronic kidney diseases，CKD) 的分期方法提出了新的建议（见附录: 慢性肾脏病）。显然，CKD 和 CRF 的含义上有相当大的重叠，前者范围更广，而后者则主要代表 CKD 患者中的 GFR 下降的那一部分群体。 CRF 的病因主要有原发性与继发性肾小球肾炎(如糖尿病肾病、高血压肾小动脉硬化、狼 疮性肾炎等)、肾小管间质病变（慢性肾盂肾炎、慢性尿酸性肾病、梗阻性肾病、药物性肾 病等）、肾血管病变、遗传性肾病（如多囊肾、遗传性肾炎）等。在发达国家，糖尿病肾病、高血压肾小动脉硬化已成为 CRF 的主要病因，在发展中国家，这两种疾病在 CRF 各种病因中仍位居原发性肾小球肾炎之后，但近年也有明显增高趋势。双侧肾动脉狭窄或闭塞所引起的“缺血性肾病”（ischemic nephropathy），在老年 CRF 的病因中占有较重要的地位。 【临床表现】 在 CRF 的不同阶段，其临床表现也各不相同。在 CRF 的代偿期和失代偿早期，病人可以 无任何症状，或仅有乏力、腰酸、夜尿增多等轻度不适；少数病人可有食欲减退、代谢性酸中毒及轻度贫血。CRF 中期以后，上述症状更趋明显。在尿毒症期，可出现急性心衰、严重高钾血症、消化道出血、中枢神经系统障碍等严重并发症，甚至有生命危险。 1. 水、电解质代谢紊乱慢性肾衰时，酸碱平衡失调和各种电解质代谢紊乱相当常见。 在这类代谢紊乱中，以代谢性酸中毒和水钠平衡紊乱最为常见。 （1）代谢性酸中毒：在部分轻中度慢性肾衰（GFR>25 ml/min，或血肌酐<350μmol/l） 患者中，部分患者由于肾小管分泌氢离子障碍或肾小管 HCO3 -的重吸收能力下降，因而可发生 正常阴离子间隙的高氯血症性代谢性酸中毒，即肾小管性酸中毒。当 GFR 降低至<25 ml/min （血肌酐>350μmol/l）时，肾衰时代谢产物如磷酸、硫酸等酸性物质因肾的排泄障碍而潴留，可发生高氯血症性（或正氯血症性）高阴离子间隙性代谢性酸中毒，即“尿毒症性酸中 206 毒”。轻度慢性酸中毒时, 多数患者症状较少，但如动脉血 HCO -3 < 15 mmol/L，则可出现明 显食欲不振、呕吐、虚弱无力、呼吸深长等。 （2）水钠代谢紊乱：主要表现为水钠潴留，或低血容量和低钠血症。肾功能不全时，
慢性肾功能不全指导原则（主要内容） 1.治疗疗效标准/目标： 预防或减缓发展的最终目的是保护慢性肾病肾功能不全的肾功能、改善肾和总生存期。 预防和延缓CKD是慢病管理中最主要的，主要有两个不同的治疗目标： 一级预防:在高风险人群中（如糖尿病、原发性高血压等）预防慢性肾脏疾病。受试者没有明显的慢性肾脏疾病的迹象，即没有任何肾损害的迹象。 二级预防:包括减缓慢性肾脏疾病进展，患者存在慢性肾脏疾病的迹象。 不希望只有代表肾病理检测，如不接受蛋白尿或肾小球滤过率(GFR)的微小变化作为一个独立的指标或构成一个独立的标志的一部分。 2.评估疗效标准的方法 肾功能的评估 血清肌酐，有或没有胱抑素C，相应的估计肾小球滤过率(GFR)(eGFR)被用于一些试验来评估肾功能和在今后的试验中也可以接受。然而,这些方法不够准确反映的全部真实的肾小球滤过率(GFR)。然而，这些方法并不足够准确地表示真实GFR的全部范围。虽然使用外源物质（碘海醇，伊马替拉或其他有效标记物）的清除来测量GFR（mGFR）可能更准确，但是在全球发展中进行关键研究的常规临床实践中正确使用的困难也得到承认。建议在预先确定的患者亚组中使用测量的GFR作为eGFR的验证性检验。由于前者更好地表征，基于肌酐的eGFR 估计目前优于基于胱抑素C的估计。不考虑用于eGFR估计的测量，需要考虑所有产生生物标志物变异性的混杂因子及其对数据解释的影响。 然而在一些情况下，GFR的精确测定被认为是必不可少的，例如当GFR的预期下降非常缓慢时，导致试验研究时间非常长（多年），或由于用于估计的生物标志物的非GFR决定因素的巨大差异来估计GFR是不可靠的，因此建议将mGFR 优先于eGFR。eGFR使用验证的方程例如肾脏疾病研究组（MDRD）或慢性肾脏疾病流行病学协作（CKD-EPI）中的饮食改变也可用于补充mGFR，特别是对于纵向观察中的多次测量。 应考虑急性血液动力学对评估GFR下降的影响。研究设计应证明急性作用
子宫内膜癌 这是美国妇产科协会（ACOG）的第149号实践指南（Practice Bulletin）。全文长达21页，现将其推荐和结论的总结翻译如下。文中数张表格附在最后。 A级证据：基于良好和一致的科学证据 ●门诊以一次性器械进行内膜活检对于绝大部分内膜癌患者而言是可靠而准确的，已经成为组织学评估内膜的首选方法。 ●宫腔镜尽管并非必须，但仍推荐和诊刮（D&C）一起进行，以识别不连续的病灶及其背景内膜。这种联合检查可以为真正的内膜癌前病变提供确诊的最佳机会，并能排除相关的内膜癌变。 ●并不需要对内膜癌患者常规进行影像学检查以评估有无转移。 ●内膜癌的初期治疗应该包括完整的手术分期（全子宫及双附件切除，盆腔及腹主动脉旁淋巴结切除，腹膜细胞学[腹腔冲洗液]的收集）。只有在和内膜癌诊疗专家（如妇科肿瘤学家）进行咨询之后，才能决定其他治疗方案以取代上述初期治疗方案。 ●应该接受将微创手术作为内膜癌患者完整手术分期的标准手术方案。 ●对于I期或II期的内膜癌，辅助性放疗可以降低局部复发率，但并不影响总体预后。 ●对于有复发高中风险的患者中，阴道短距放疗应该成为代替全盆腔放疗的首选辅助治疗。 ●对于晚期内膜癌患者，化疗能够改善患者预后。 ●经过对激素治疗利弊的充分咨询后，对于早期内膜癌患者可以考虑激素治疗绝经后症状。 B级证据：基于有限的或不一致的科学证据 ●对于绝经后阴道流血、阴道超声检查内膜厚度≤4mm的女性，并不需要行内膜活检。 ●绝经后阴道流血、阴道超声检查内膜厚度> 4mm的女性，以及内膜厚度无法充分检查的女性，应该考虑其他评估方案，如超声造影术，门诊宫腔镜检查或内膜活检。 ●由于某些内膜癌（特别是II型内膜癌）的罕见病例其内膜厚度可以≤3 mm，因此对于持续或反复出血的情况无论内膜厚度多少，都应该立即行组织学评估。 ●对于内膜癌患者，机器人辅助的腹腔镜分期是可行且安全的，可以作为传统腹腔镜的替代方案。 ●淋巴结切除也许可以改变或消除辅助治疗的必要及其相关患病率。 ●已经发现，理想的细胞减灭术（有不同的定义，残余病灶≤1 cm或2 cm）能够改善晚期或复发性内膜癌患者的无进展生存和总体生存。 ●对于有大块病灶残余的女性，以紫杉醇和卡铂方案进行化疗，其效果与文献中报道的其他方案类似，但毒副反应更少一些。 C级证据：主要基于共识和专家观点 ●低级别病变的患者（也就是说1级或2级内膜癌，肌层浸润深度小于50%，肿瘤直径≤2 cm）淋巴结转移的风险似乎较低，也许不需要系统性的淋巴结切除。 ●以影像学在术前评估疾病转移（CT，核磁，PET/CT），检查血清CA125，或二者联合检查，在某些特定情况下也许具有临床重要性：如患者由于合并症而很难施行手术；如患者症状提示病灶转移到非常见部位（如骨骼和中枢神经）；如术前组织学证实高级别病变（包括3级的内膜样癌，乳头状浆液性癌，透明细胞癌和癌肉瘤）。 ●在某些选择性的、手术患病率风险较高的早期内膜癌患者中，阴式子宫切除可能是合适的治疗方案.
美国临床肿瘤学会/美国病理学医师学院乳腺癌ER/PR免疫组织化学检测指南简介 傅静，刘裔莎，步宏 美国临床肿瘤学会（ASCO）/美国病理学医师学院（CAP）于2010年5月发布了乳腺癌ER/PR免疫组织化学（IHC）检测指南，目的在于改善ER/PR免疫组化检测的准确性，提高对内分泌治疗效果的预测价值【1】。 雌激素受体（ER）在乳腺癌的发生、发展过程起重要作用，是乳腺癌重要的生物学标记。孕激素受体（PR）编码基因由经ER介导的雌激素调控，PR阳性表达是ER功能的体现。大量临床试验证实ER和/或PR阳性表达的乳腺癌患者能获益于内分泌治疗，显著改善预后。为筛选合适的患者进行内分泌治疗，提高内分泌治疗的有效性，也使其他患者免受内分泌治疗可能导致的副作用及不必要的经济负担，准确的ER/PR检测结果至关重要。现常规使用IHC检测ER/PR 表达状态，但该检测方法尚未实现标准化，约有20%的ER和PR免疫组化检测结果不正确（假阳性或假阴性），主要的影响原因涉及到染色前因素，阳性界值及结果判读等方面。 一、检测时机 所有原发和复发的浸润性乳腺癌需行ER和PR检测。DCIS病例由患者和临床医师讨论决定是否进行ER和PR检测。 二、染色前 与我们已较熟悉的HER2检测一样【2】，用于ER/PR检测的标本离体后应尽快固定，从离体到固定的时间不能超过1h。标本固定选择至少10倍体积的10%中性缓冲福尔马林液，固定时间6-72h。肿瘤大体检查及边界确定后，标本需每间隔5mm切开，并用纱布或滤纸将相邻组织分开保证固定液充分渗透和固定。取材时如果肿瘤明确，应同时取一小块正常乳腺组织放入包埋盒，作为肿瘤的阳性对照。如果标本来源较远，运送前将肿瘤对剖开，放入足量固定液。记录标本离体时间，开始固定时间，固定持续时间及固定类型。用于ER/PR免疫组化检作者单位：610041 成都，四川大学华西医院病理科 通信作者：步宏（Email: hongbu@https://www.doczj.com/doc/9a7059207.html,)
慢性肾脏病蛋白营养治疗专家共识 发表者：杨爱成(访问人次：962) 一、营养治疗对慢性肾脏病的意义 限制蛋白质饮食是治疗慢性肾脏病(CKD) 、特别是慢性肾衰竭的一个重要环节。在施行低蛋白饮食、尤其极低蛋白饮食治疗时,为防止营养不良,建议给病人同时补充复方α- 酮酸制剂或必需氨基酸制剂。但是,已有研究表明,补充复方α- 酮酸制剂在延缓肾损害进展上疗效优于必需氨基酸制剂。研究表明,低蛋白饮食加复方α- 酮酸制剂治疗有如下益处: ①减轻氮质血症,改善代谢性酸中毒; ②补充机体所缺必需氨基酸,改善蛋白质代谢; ③减轻胰岛素抵抗,改善糖代谢; ④提高脂酶活性,改善脂代谢; ⑤降低高血磷,改善低血钙,减轻继发性甲状旁腺功能亢进; ⑥减少蛋白尿排泄,延缓CKD 进展。 [附录1 :CKD 定义及分期] 二、营养治疗的实施方案 (一) 透析前慢性肾脏病(非糖尿病肾病) 病人 1.1 蛋白入量 CKD 第1 、2 期原则上宜减少饮食蛋白,推荐蛋白入量0.8g/ kg·d。从CKD 第3 期起( GFR < 60ml/ min·1.73m2) 即应开始低蛋白饮食治疗,推荐蛋白入量0.6g/ kg·d ,并可补充复方α- 酮酸制剂0.12g/ kg·d。若GFR 已重度下降( < 25ml/ min·1.73m2 ) ,且病人对更严格蛋白限制能够耐受,则蛋白入量还可减至014g/ kg·d左右,并补充复方α- 酮酸制剂0.20g/ kg·d。由于复方α-酮酸制剂含钙(每片含钙50mg) ,因此服药量较大、尤其与活性维生素D 同时服用时要监测血钙,谨防高钙血症发生。在低蛋白饮食中,约50 %蛋白应为高生物价蛋白。2.1 热量摄入 实施低蛋白饮食治疗时, 热量摄入需维持于30 ～35kcal/ kg·d。 3.1 其它营养素 各种维生素及叶酸应充分补充。当出现高磷血症时磷入量应限制在800mg/ d 以下(最佳入量为500mg/ d) 。 (二) 透析前糖尿病肾病病人 1.1 蛋白入量 从出现显性蛋白尿起即应减少饮食蛋白,推荐蛋白入量0.8g/ kg·d。从GFR 下降起,即应实施低蛋白饮食,推荐蛋白入量0.6g/ kg·d ,并可同时补充复方α- 酮酸制剂0.12g/ kg·d。 2.1 热量摄入 实施低蛋白饮食治疗时,病人的热量摄入应基本与前述非糖尿病肾病病人相似,但是,肥胖的2 性糖尿病病人需适当限制热量(总热量摄入可比上述推荐量减少25 0～500kcal/ d) ,直至达到标准体重。由于病人蛋白入量(仅占总热量的～10 %左右) 及脂肪入量(仅能占总热量的～30 %均被限制,故所缺热量往往只能从碳水化合物补充,必要时应注射胰岛素保证碳水化合物利用。 3.1 其它营养素 与非糖尿病肾病CKD 病人要求相同。 [附录2 : GFR 计算公式] (三) 血液透析和腹膜透析病人 维持性血液透析病人推荐蛋白入量为112g/ kg·d ,当病人合并高分解状态的急性疾病时, 蛋白入量应增加至113g/ kg·d ;维持性腹膜透析病人推荐蛋白入量